The suppressing effects of BTG3 expression on aggressive behaviors and phenotypes of colorectal cancer: An in vitro and vivo study
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Hua-Chuan Zheng1, Hao-Yu He1, Ji-Cheng Wu1, Jing Li2, Shuang Zhao1, Gui-Feng Zhao1, Hua-Mao Jiang2, Xue-Wen Yu2, Zhi-Jie Li1
1Department of Experimental Oncology and Animal Center, Shengjing Hospital of China Medical University, Shenyang 110004, China
2Jinzhou Medical University, Jinzhou 121001, China
Hua-Chuan Zheng, email: email@example.com
Keywords: colorectal cancer, BTG3, pathobiological behaviors, aggressive phenotypes, gene therapy
Received: December 06, 2016 Accepted: January 11, 2017 Published: February 17, 2017
Here, we found that down-regulated expression of BTG3 might be positively correlated with colorectal carcinogenesis and its overexpression suppressed proliferation, glycolysis, mitochondrial respiration, cell cycle progression, migration, and invasion, and induced apoptosis, senescence and differentiation in SW480 and SW620 cells. After treated with cisplatin, MG132, paclitaxel and SAHA, BTG3 transfectants exhibited lower viability and higher apoptosis than the control in both time- and dose-dependent manners. BTG3 overexpression up- regulated the protein expression of Cyclin E, p16, p27, NF-κB, p38α/β, XIAP, Bcl-2, ATG14 and p53, but down-regulated the mRNA expression of MRP1, BCRP, and mTOR in SW480 and SW620 cells. BTG3 overexpression inhibited tumor growth of SW620 cells by suppressing proliferation and inducing apoptosis. It was suggested that down-regulated BTG3 expression might be considered as a marker for colorectal carcinogenesis. BTG3 overexpression might reverse the aggressive phenotypes and be employed as a potential target for gene therapy of colorectal cancer.
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